OBJECTIVE: Clinical symptoms and laboratory indices for acute inflammatory demyelinating polyneuropathy (AIDP), a variant of Guillain-Barré syndrome, and acute-onset chronic inflammatory demyelinating polyneuropathy (A-CIDP) were analyzed to identify factors that could contribute to early differential diagnosis.
METHODS: A retrospective chart review was performed on 44 AIDP and 44 A-CIDP patients looking for any demographic characteristics, clinical manifestations or laboratory parameters that might differentiate AIDP from acutely presenting CIDP.
RESULTS: In Guillain-Barré syndrome patients (N = 63), 69.84% (N = 44) were classified as having AIDP, 19.05% (N = 12) were found to have acute motor axonal neuropathy, 6.35% (N = 4) were found to have acute motor and sensory axonal neuropathy, and 4.76% (N = 3) were found to have Miller Fisher syndrome. Serum uric acid (UA) was higher in A-CIDP patients (329.55 ± 72.23 μmol/L) than in AIDP patients (221.08 ± 71.32 μmol/L) (p = 0.000). Receiver operating characteristic analyses indicated that the optimal UA cutoff was 283.50 μmol/L. Above this level, patients were more likely to present A-CIDP than AIDP (specificity 81.80%, sensitivity 81.80%). During the follow-up process, serum samples were effectively collected from 19 AIDP patients during the rehabilitation phase and 28 A-CIDP patients during the remission stage, and it was found that UA levels were significantly increased in A-CIDP (remission) (298.9 ± 90.39 μmol/L) compared with AIDP (rehabilitation) (220.1 ± 108.2 μmol/L, p = 0.009).
CONCLUSIONS: These results suggest that serum UA level can help to differentiate AIDP from A-CIDP with high specificity and sensitivity, which is helpful for early diagnosis and guidance of treatment.

BACKGROUND: Guillain-Barré syndrome (GBS), as the most common cause of acute flaccid paralysis worldwide, is considered a part of a clinical spectrum in which discrete, complete, or incomplete forms of GBS and overlapping syndromes lie on the basis of their clinical features. The term overlapping Miller Fisher syndrome (MFS)/GBS is used when patients with MFS also suffer from progressive motor weakness of the limbs. Anti-ganglioside GQ1b has been specifically associated with MFS and ophthalmoplegia.
METHODS: Here, we report a Chinese girl who was diagnosed with overlapping MFS/GBS showing acute flaccid paralysis of all four limbs, sensory symptoms, cranial nerve dysfunction, autonomic involvement, ophthalmoplegia, and ataxia. She had high serum and cerebrospinal fluid titres of monospecific anti-GM4 IgG antibody instead of anti-GQ1b antibody in the acute phase.
CONCLUSIONS: Anti-GM4 antibodies usually coexist with other antiganglioside antibodies, leading to missed diagnoses. The findings of the present study show that antibodies to ganglioside GM4 may in overlapping MFS/GBS as the lone immunological factors.

BACKGROUND: Anti-ganglioside antibodies (AGA) play an essential role in the development of Miller-Fisher syndrome (MFS). The positive rate of ganglioside antibodies was exceptionally high in MFS, especially anti-GQ1b antibodies. However, the presence of other ganglioside antibodies does not exclude MFS.
METHODS: We present a 48-year-old male patient who suddenly developed dizziness, visual rotation, nausea, and vomiting accompanied by unsteady gait and diplopia for 3 days before presentation to our clinic.
METHODS: On physical examination, the patient\'s right eye could not fully move to the right side and horizontal nystagmus was found. Coordination was also impaired in the upper and lower extremities with dysmetria and dysdiadochokinesia. The electromyography and cerebrospinal fluid examination results were normal. The serum anti-GQlb antibody test results were negative. However, serum anti-GD1b IgM and anti-GM1 IgM antibodies were positive. Meanwhile, the anti-thyroid peroxidase antibody was >600.00 IU/mL (0.00-34.00), and the anti-SS-A/Ro52 antibody was positive. He was diagnosed with MFS.
METHODS: The patient received IVIg treatment for 5 days (0.4 g/kg/day) from day 2 to day 6 of hospitalization. On the 7th day of admission, the patient was administered intravenous methylprednisolone (500 mg/day), which was gradually reduced.
RESULTS: The patient\'s symptoms improved after treatment with immunoglobulins and hormones.
CONCLUSIONS: We report a case of MFS with positive anti-GD1b and anti-GM1 antibodies combined with multiple autoimmune antibodies. Positive ganglioside antibodies may be used as supporting evidence for the diagnosis; however, the diagnosis of MFS is more dependent on clinical symptoms.

Guillain-Barré syndrome (GBS) and Miller Fisher syndrome (MFS) are acute immune-mediated peripheral neuropathies. In addition to their classic presentations, a variety of other signs and symptoms have been reported; however, headache appears to be relatively uncommon. We describe a 53-year-old woman who presented with acute bulbar palsy as the first symptom of overlapping MFS/GBS accompanied by severe headache. The first important clinical impairment of the patient was acute bulbar palsy along with prominent headache, without limb weakness. Although her initial diagnosis was acute bulbar palsy plus, she subsequently developed lower limb diffuse weakness, and her final clinical diagnosis was overlapping MFS/GBS. Anti-ganglioside antibodies were positive for anti-GQ1b and anti-GT1a immunoglobulin G. The patient received intravenous immunoglobulin on day 2 of admission. Early identification of these overlapping syndromes is important for the management of patients, to avoid respiratory failure or severe weakness with axonal degeneration. We therefore remind clinicians of the importance of further examination in patients with headache and acute bulbar palsy of unknown origin.

OBJECTIVE: We aimed to determine the clinical features of Miller Fisher syndrome (MFS) in southern China and compare them with those presenting in other countries.
METHODS: We collected the medical records of patients diagnosed with MFS during 2013-2016. We analyzed the age, sex, onset season, precursor events, clinical symptoms and signs, findings of nerve conduction studies (NCS), cerebrospinal fluid (CSF), therapeutic remedies, nadir time, and length of hospital stay of patients with MFS in southern China. We concurrently compared the differences between urban and rural areas and between patients with incomplete ophthalmoplegia (IO) and complete ophthalmoplegia (CO).
RESULTS: The study enrolled 72 patients: 36 from rural areas and 36 from urban areas, and 50 males and 22 females. The mean age at onset was 47.72 years, and 30 (41.7%) and 21 (29.2%) patients developed MFS in spring and winter, respectively. The typical triad of ophthalmoplegia, ataxia, and areflexia was observed in 50 (69.4%) patients. A history of upper respiratory tract infection 1 week before onset was found in 52.8% of the patients, while 5.6% experienced gastrointestinal infections and 48 (73.8%) exhibited albuminocytological dissociation in the CSF study. Only 26 (36.1%) patients presented abnormalities in NCS. Moreover, restricted outward eyeball movement presented in 83.5% of the patients with classic MFS and acute ophthalmoplegia, and bilateral symmetrical ophthalmoplegia presented in 64.2%. With the exception of the higher proportion of NCS abnormalities in urban areas (47.2% vs. 25.0%), urban and rural differences were insignificant regarding sex ratio, age at onset, high-incidence season, precursor events, disease characteristics, and albuminocytological dissociation in the CSF. Furthermore, patients with CO were older than those with IO (64.53±7.69 vs. 43.19±14.40 years [mean±standard deviation], p<0.001).
CONCLUSIONS: The patients with MFS were mostly male and middle-aged, and most presented in winter and (especially) spring. More than half of the patients had clear precursor events, most of which were classic MFS with the typical triad. More than 70% of the patients presented albuminocytological dissociation in the CSF. NCS abnormalities were uncommon in MFS. The age at onset was lower in patients with IO than in patients with CO; bilateral symmetrical extraocular muscle paralysis was the most common symptom, and the external rectus was the most frequently involved muscle.

BACKGROUND: Anti-GQ1b antibody syndrome is a rare autoimmune neuropathy, and atypical cases are even more rare, only a few cases have been reported. Anti-GQ1b antibody syndrome is difficult in early diagnosis and prone to misdiagnosis. Generally,in children with anti-GQ1b antibody syndrome,extraocular muscle paralysis is the initial symptom. However, anti-GQ1b antibody syndrome with vomiting as the initial symptom followed by abnormal gait has not been reported.
METHODS: We reported a case of anti-GQ1b antibody syndrome with vomiting as the initial symptom, followed by abnormal gait. One day after vomiting, the child developed abnormal gait, which primarily manifested as a slight tilt of the upper body during walking as well as an opening and swaying of the legs at fast walking paces,then progressively aggravated, and finally he could not stand on his own.In the auxiliary examination, cerebrospinal fluid routine,biochemical and metagenomic Next-Generation Sequencing (DNA and RNA), brain + spinal cord contrast magnetic resonance imaging (MRI),magnetic Resonance angiography (MRA) and diffusion-weighted image (DWI), hip and knee joint ultrasound showed normal results. Anti-GQ1b antibody syndrome was not confirmed until the positive anti-GQ1b IgG antibody was detected in the serum. After treatment with intravenous immunoglobulin (IVIG) and glucocorticoid, the child recovered well, and a 3-month outpatient follow-up showed that the child was able to walk normally.
CONCLUSIONS: There are no previous reports of anti-GQ1b antibody syndrome with vomiting as the initial symptom, followed by abnormal gait. Therefore, this valuable case contributes to expanding the database of clinical manifestation of anti-GQ1b antibody syndrome, so as to improve pediatricians\' awareness about such rare diseases and reduce misdiagnosis.

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To investigate CSF findings in relation to clinical and electrodiagnostic subtypes, severity, and outcome of Guillain-Barré syndrome (GBS) based on 1,500 patients in the International GBS Outcome Study.
Albuminocytologic dissociation (ACD) was defined as an increased protein level (>0.45 g/L) in the absence of elevated white cell count (<50 cells/μL). We excluded 124 (8%) patients because of other diagnoses, protocol violation, or insufficient data. The CSF was examined in 1,231 patients (89%).
In 846 (70%) patients, CSF examination showed ACD, which increased with time from weakness onset: ≤4 days 57%, >4 days 84%. High CSF protein levels were associated with a demyelinating subtype, proximal or global muscle weakness, and a reduced likelihood of being able to run at week 2 (odds ratio [OR] 0.42, 95% CI 0.25-0.70; p = 0.001) and week 4 (OR 0.44, 95% CI 0.27-0.72; p = 0.001). Patients with the Miller Fisher syndrome, distal predominant weakness, and normal or equivocal nerve conduction studies were more likely to have lower CSF protein levels. CSF cell count was <5 cells/μL in 1,005 patients (83%), 5-49 cells/μL in 200 patients (16%), and ≥50 cells/μL in 13 patients (1%).
ACD is a common finding in GBS, but normal protein levels do not exclude this diagnosis. High CSF protein level is associated with an early severe disease course and a demyelinating subtype. Elevated CSF cell count, rarely ≥50 cells/μL, is compatible with GBS after a thorough exclusion of alternative diagnoses.
This study provides Class IV evidence that CSF ACD (defined by the Brighton Collaboration) is common in patients with GBS.

This study aimed to retrospectively analyze reported Guillain-Barré syndrome (GBS) cases that occurred after COVID-19 vaccination.
Case reports of GBS following COVID-19 vaccination that were published before May 14, 2022, were retrieved from PubMed. The cases were retrospectively analyzed for their basic characteristics, vaccine types, the number of vaccination doses before onset, clinical manifestations, laboratory test results, neurophysiological examination results, treatment, and prognosis.
Retrospective analysis of 60 case reports revealed that post-COVID-19 vaccination GBS occurred mostly after the first dose of the vaccination (54 cases, 90%) and was common for DNA vaccination (38 cases, 63%), common in middle-aged and elderly people (mean age: 54.5 years), and also common in men (36 cases, 60%). The mean time from vaccination to onset was 12.3 days. The classical GBS (31 cases, 52%) was the major clinical classification and the AIDP subtype (37 cases, 71%) was the major neurophysiological subtype, but the positive rate of anti-ganglioside antibodies was low (7 cases, 20%). Bilateral facial nerve palsy (76% vs 18%) and facial palsy with distal paresthesia (38% vs 5%) were more common for DNA vaccination than for RNA vaccination.
After reviewing the literature, we proposed a possible association between the risk of GBS and the first dose of the COVID-19 vaccines, especially DNA vaccines. The higher rate of facial involvement and a lower positive rate of anti-ganglioside antibodies may be a characteristic feature of GBS following COVID-19 vaccination. The causal relationship between GBS and COVID-19 vaccination remains speculative, more research is needed to establish an association between GBS and COVID-19 vaccination. We recommend surveillance for GBS following vaccination, because it is important in determining the true incidence of GBS following COVID-19 vaccination, as well as in the development of a more safer vaccine.

Miller-Fisher syndrome (MFS) is a rare variant of Guillain-Barré syndrome (GBS) manifesting as the triad of ataxia, areflexia, and ophthalmoplegia. With the extensive 2019 coronavirus disease (COVID-19) immunization program, cases of GBS or MFS following vaccination are increasingly being reported. A 64-y-old Chinese man presented with new-onset paresthesia of the extremities, bilateral abduction limitation, right facial palsy, areflexia of bilateral lower limbs, and left-dominant limb ataxia 12 d after the second dose of inactivated vaccine against COVID-19. Cerebrospinal fluid analysis indicated albumin-cytological dissociation and was positive for anti-GQ1b IgG and anti-GT1b IgG. Nerve conduction studies of limbs showed evidence of axonal neuropathy with reduced sensory amplitudes. Based on the clinical presentations, temporal progression of symptoms, and laboratory findings, the diagnosis of MFS-GBS overlap syndrome was made. The patient was treated with intravenous immunoglobulin and acupuncture and made a complete recovery 54 d after the onset of his initial neurological signs. To the best of our knowledge, we report the first case of MFS-GBS overlap syndrome following the inactivated COVID-19 vaccination. However, a coincidental relationship with this inactivated vaccine cannot be excluded. Although the benefits of COVID-19 vaccination largely outweigh its risk and the prognosis of MFS is generally favorable, a close surveillance of neurological complications post-COVID-19 vaccination is always necessary, considering its potentially disabling and lethal effects on vaccinated populations.